模块化职务分析

章总结了职务分析方法在我国的应用情况，分析了需求特点，引入模块化的思想，提出了新的职务分析方法——模块化职务分析，认为职务分析的关键就是将工作中的各项任务进行整理，组成不同的工作模块。建立计算机辅助管理系统，时时调整、修改工作模块，对工作模块进行组合，形成职务，从而使职务分析趋于动态化。     

俄气南供与天然气利用规划

介绍了俄气南供的供气方案，讨论了天然气的市场调查和价格的确定等问题。     

用干涉环法分析CSTN-LCD盒厚均匀性

总结了CSTN空盒及实盒对应干涉环的一些情况,用劈尖原理推算了空盒干涉环明、暗环对应盒厚差值等,推算值与实测值基本相符;提出用实盒干涉环规整程度分析CSTN-LCD 盒厚均匀性或颜色均匀性,由此可以相应深入分析产生盒厚不匀的相关原因.     

邯钢西区煤气管网改造及效果分析

介绍了邯钢为减少煤气放散，节约能源，采用环网供应混合煤气的有效方法。提高了供气可靠性，取得了很好的经济效益。     

与客户建立互惠互利长期稳定的营销关系

在我国加入WTO之后，国内钢铁企业与经销商之间如何实现互惠互利，并建立起长期稳定的营销关系。     

白云鄂博主矿开拓运输工艺转换有关问题的探讨

本文对白云鄂博主矿采场铁公路联合运输向公路运输转换位置是否确定为1638m水平以及运输工艺转换过程中相关问题进行分析论证，提出主矿采场铁路至少可向下延深一个水平，技术上可行，节约运费千万元以上。     

Bilateral loss of vestibular function: clinical findings in 53 patients

The clinical presentations and aetiologies of a series of 53 cases of bilateral vestibular failure (BVF) seen by the authors over a decade were evaluated by retrospective review of the medical records. Thirty-nine per cent of patients had associated neurological disease; 13% had a progressive cerebellar syndrome with disabling gait ataxia, abnormal eye movements and cerebellar atrophy on neuro-imaging. BVF was usually unsuspected. Nine per cent had cranial or peripheral neuropathies and in this group there was no abnormality of brain stem/cerebellar oculomotor function, but hearing loss was common. Eleven per cent revealed BVF and hearing loss secondary to meningitis, and 6% had other neurological disorders. Idiopathic BVF was found in 21% of cases, characterised by paroxysmal vertigo and/or oscillopsia, but no abnormal clinical signs. Gentamicin ototoxicity accounted for a further 17%, while autoimmune disease was present in 9% of patients. Otological or neoplastic disease was diagnosed in the remaining 13% of patients. It was concluded that neurological, audiological and ocular motor assessments allow the probable cause of BVF to be defined in approximately 80% of cases. A group of BVF related to autoimmune pathologies is reported for the first time, indicating the need for immunological screening. Idiopathic BVF may present with only minor visual or vestibular symptoms, while in patients with cerebellar degeneration, BVF may be unsuspected and, thus, underdiagnosed.     

Mannolipid donor specificity of glycosylphosphatidylinositol mannosyltransferase-I (GPIMT-I) determined with an assay system utilizing mutant CHO-K1 cells

The microsomal enzyme glycosylphosphatidylinositol mannosyltransferase I (GPIMT-I) catalyses the transfer of a mannosyl residue from beta-mannosylphosphoryldolichol (beta-Man-P-Dol) to glucosamine-alpha(1,6)(acyl)phosphatidylinositol (GlcN-aPI) to form Man alpha(1,4)GlcN-aPI (ManGlcN-aPI), an intermediate in glycosylphosphatidylinositol (GPI) synthesis. While the transfer of [3H]mannosyl units to endogenous GlcN-aPI was not seen when membrane fractions from normal Chinese hamster ovary (CHO) K1 cells were incubated with exogenous [3H]Man-P-Dol, GPIMT-I activity could be characterized with an in vitro enzyme assay system employing membrane fractions from Lec15 or Lec35 cells. These CHO cell mutants apparently contain elevated levels of endogenous GlcN-aPI due to the inability to synthesize (Lec15) or utilize (Lec35) beta-Man-P-Dol in vivo. The presence of a saturated alpha-isoprene unit in the dolichyl moiety is required for optimal GPIMT-I activity since beta-mannosylphosphorylpolyprenol (beta-Man-P-Poly), which contains a fully unsaturated polyisoprenyl chain, was only 50% as effective as beta-[3H]Man-P-Dol as a mannosyl donor. When beta-[3H]-Man-P-Dol and alpha-[3H]Man-P-Dol were compared as substrates, GPIMT-I exhibited a strict stereospecificity for the mannolipid containing the beta-mannosyl-phosphoryl linkage. beta-[3H]Man-P-dolichols containing 11 or 19 isoprenyl units were equally effective substrates for GPIMT-I. Membrane fractions from Lec 9, a CHO mutant that apparently lacks polyprenol reductase activity and synthesizes very little beta-Man-P-Dol, but accumulates beta-Man-P-Poly, synthesized no detectable Man-GlcN-aPI when incubated with beta-[3H]Man-P-Dol in vitro. This indirect assay suggests that GlcN-aPI does not accumulate in Lec 9 cells, possibly because it is mannosylated via beta-Man-P-Poly, or perhaps the small amount of Man-P-Dol formed by the mutant in vivo.(ABSTRACT TRUNCATED AT 250 WORDS)